Robust and Low-Complexity Timing Synchronization for DCO-OFDM LiFi Systems

Personal use of this material is permitted. Permission from IEEE must be obtained for all other uses, in any current or future media, including reprinting/republishing this material for advertising or promotional purposes, creating new collective works, for resale or redistribution to servers or lists, or reuse of any copyrighted component of this work in other works.Light fidelity (LiFi), using light emitting devices such as light emitting diodes (LEDs) which are operating in the visible light spectrum between 400 and 800 THz, provides a new layer of wireless connectivity within existing heterogeneous radio frequency wireless networks. Link data rates of 10 Gbps from a single transmitter have been demonstrated under ideal laboratory conditions. Synchronization is one of these issues usually assumed to be ideal. However, in a practical deployment, this is no longer a valid assumption. Therefore, we propose for the first time a low-complexity maximum likelihood-based timing synchronization process that includes frame detection and sampling clock synchronization for direct current-biased optical orthogonal frequency division multiplexing LiFi systems. The proposed timing synchronization structure can reduce the high-complexity two-dimensional search to two low-complexity one-dimensional searches for frame detection and sampling clock synchronization. By employing a single training block, frame detection can be realized, and then sampling clock offset (SCO) and channels can be estimated jointly. We propose three frame detection approaches, which are robust against the combined effects of both SCO and the low-pass characteristic of LEDs. Furthermore, we derive the Cramér-Rao lower bounds (CRBs) of SCO and channel estimations, respectively. In order to minimize the CRBs and improve synchronization performance, a single training block is designed based on the optimization of training sequences, the selection of training length, and the selection of direct current (DC) bias. Therefore, the designed training block allows us to analyze the trade-offs between estimation accuracy, spectral efficiency, energy efficiency, and complexity. The proposed timing synchronization mechanism demonstrates low complexity and robustness benefits and provides performance significantly better than achieved with existing methods.Peer reviewe

Reactivating aberrantly hypermethylated p15 gene in leukemic T cells by a phenylhexyl isothiocyanate mediated inter-active mechanism on DNA and chromatin

<p>Abstract</p> <p>Background</p> <p>We have previously demonstrated that phenylhexyl isothiocyanate (PHI), a synthetic isothiocyanate, inhibits histone deacetylases and remodels chromatins to induce growth arrest in HL-60 myeloid leukemia cells in a concentration-dependent manner.</p> <p>Methods</p> <p>To investigate the effect of PHI, a novel histone deacetylases inhibitor (HDACi), on demethylation and activation of transcription of <it>p15 </it>in acute lymphoid leukemia cell line Molt-4, and to further decipher the potential mechanism of demethylation, DNA sequencing and modified methylation specific PCR (MSP) were used to screen <it>p15</it>-M and <it>p15</it>-U mRNA after Molt-4 cells were treated with PHI, 5-Aza and TSA. DNA methyltransferase 1 (DNMT1), 3A (DNMT3A), 3B (DNMT3B) and <it>p15 </it>mRNA were measured by RT-PCR. P15 protein, acetylated histone H3 and histone H4 were detected by Western Blot.</p> <p>Results</p> <p>The gene <it>p15 </it>in Molt-4 cells was hypermethylated and inactive. Hypermethylation of gene <it>p15 </it>was attenuated and <it>p15 </it>gene was activated de novo after 5 days exposure to PHI in a concentration-dependent manner. DNMT1 and DNMT3B were inhibited by PHI (P < 0.05). Alteration of DNMT3A was not significant at those concentrations. Acetylated histone H3 and histone H4 were accumulated markedly after exposure to PHI.</p> <p>Conclusion</p> <p>PHI could induce both DNA demethylation and acetylated H3 and H4 accumulation in Molt-4 cells. Hypermethylation of gene <it>p15 </it>was reversed and <it>p15 </it>transcription could be reactivated de novo by PHI.</p

Dual-agonist occupancy of orexin receptor 1 and cholecystokinin A receptor heterodimers decreases G-protein-dependent signaling and migration in the human colon cancer cell line HT-29

The orexin (OX1R) and cholecystokinin A (CCK1R) receptors play opposing roles in the migration of the human colon cancer cell line HT-29, and may be involved in the pathogenesis and pathophysiology of cancer cell invasion and metastasis. OX1R and CCK1R belong to family A of the G-protein-coupled receptors (GPCRs), but the detailed mechanisms underlying their functions in solid tumor development remain unclear. In this study, we investigated whether these two receptors heterodimerize, and the results revealed novel signal transduction mechanisms. Bioluminescence and Förster resonance energy transfer, as well as proximity ligation assays, demonstrated that OX1R and CCK1R heterodimerize in HEK293 and HT-29 cells, and that peptides corresponding to transmembrane domain 5 of OX1R impaired heterodimer formation. Stimulation of OX1R and CCK1R heterodimers with both orexin-A and CCK decreased the activation of Gαq, Gαi2, Gα12, and Gα13 and the migration of HT-29 cells in comparison with stimulation with orexin-A or CCK alone, but did not alter GPCR interactions with β-arrestins. These results suggest that OX1R and CCK1R heterodimerization plays an anti-migratory role in human colon cancer cells. [Abstract copyright: Copyright © 2017. Published by Elsevier B.V.

Individual phosphorylation sites at the C-terminus of the apelin receptor play different roles in signal transduction

The apelin and Elabela proteins constitute a spatiotemporal double-ligand system that controls apelin receptor (APJ) signal transduction. Phosphorylation of multiple sites within the C-terminus of APJ is essential for the recruitment of β-arrestins. We sought to determine the precise mechanisms by which apelin and Elabela promote APJ phosphorylation, and to elucidate the influence of β-arrestin phosphorylation on G-protein-coupled receptor (GPCR)/β-arrestin-dependent signaling. We used techniques including mass spectrometry (MS), mutation analysis, and bioluminescence resonance energy transfer (BRET) to evaluate the role of phosphorylation sites in APJ-mediated G-protein-dependent and β-dependent signaling. Phosphorylation of APJ occurred at five serine residues in the C-terminal region (Ser335, Ser339, Ser345, Ser348 and Ser369). We also identified two phosphorylation sites in β-arrestin1 and three in β-arrestin2, including three previously identified residues (Ser412, Ser361, and Thr383) and two new sites, Tyr47 in β-arrestin1 and Tyr48 in β-arrestin2. APJ mutations did not affect the phosphorylation of β-arrestins, but it affects the β-arrestin signaling pathway, specifically Ser335 and Ser339. Mutation of Ser335 decreased the ability of the receptor to interact with β-arrestin1/2 and AP2, indicating that APJ affects the β-arrestin signaling pathway by stimulating Elabela. Mutation of Ser339 abolished the capability of the receptor to interact with GRK2 and β-arrestin1/2 upon stimulation with apelin-36, and disrupted receptor internalization and β-arrestin-dependent ERK1/2 activation. Five peptides act on distinct phosphorylation sites at the APJ C-terminus, differentially regulating APJ signal transduction and causing different biological effects. These findings may facilitate screening for drugs to treat cardiovascular and metabolic diseases

DavarOCR: A Toolbox for OCR and Multi-Modal Document Understanding

This paper presents DavarOCR, an open-source toolbox for OCR and document understanding tasks. DavarOCR currently implements 19 advanced algorithms, covering 9 different task forms. DavarOCR provides detailed usage instructions and the trained models for each algorithm. Compared with the previous opensource OCR toolbox, DavarOCR has relatively more complete support for the sub-tasks of the cutting-edge technology of document understanding. In order to promote the development and application of OCR technology in academia and industry, we pay more attention to the use of modules that different sub-domains of technology can share. DavarOCR is publicly released at https://github.com/hikopensource/Davar-Lab-OCR.Comment: Short paper, Accept by ACM MM202

Global warming and shifts in cropping systems together reduce China's rice production

Climate warming is widely expected to affect rice yields, but results are equivocal and variation in rice cropping systems and climatic conditions complicates country-scale yield assessments. Here we show, through meta–a- nalysis of field warming experiments, that yield responses to warming differ strongly between China's rice cropping systems. Whereas warming increases yields in “single rice” systems, it decreases yields in “middle rice” systems and has contrasting effects for early and late rice in “double rice” systems. We further show that the contribution of these cropping systems to China's total rice production has shifted dramatically over recent decades. We estimate that if the present structure of rice cropping systems persists, warming will reduce China's total rice production by 5.0% in 2060. However, if the recent decline in the area of double rice systems con- tinues, China's rice production may decrease by 13.5%. Our results underline the need for maintaining the current area of China's “double rice” cropping system and for technological innovations in multiple rice cropping systems to ensure food security in a warming climate

Disruption of 5-hydroxytryptamine 1A receptor and orexin receptor 1 heterodimer formation affects novel G protein-dependent signaling pathways and has antidepressant effects in vivo

G protein-coupled receptor (GPCR) heterodimers are new targets for the treatment of depression. Increasing evidence supports the importance of serotonergic and orexin-producing neurons in numerous physiological processes, possibly via a crucial interaction between 5-hydroxytryptamine 1A receptor (5-HT1AR) and orexin receptor 1 (OX1R). However, little is known about the function of 5-HT1AR/OX1R heterodimers. It is unclear how the transmembrane domains (TMs) of the dimer affect its function and whether its modulation mediates antidepressant-like effects. Here, we examined the mechanism of 5-HT1AR/OX1R dimerization and downstream G protein-dependent signaling. We found that 5-HT1AR and OX1R form constitutive heterodimers that induce novel G protein-dependent signaling, and that this heterodimerization does not affect recruitment of β-arrestins to the complex. In addition, we found that the structural interface of the active 5-HT1AR/OX1R dimer transforms from TM4/TM5 in the basal state to TM6 in the active conformation. We also used mutation analyses to identify key residues at the interface (5-HT1AR R1514.40, 5-HT1AR Y1985.41, and OX1R L2305.54). Injection of chronic unpredictable mild stress (CUMS) rats with TM4/TM5 peptides improved their depression-like emotional status and decreased the number of endogenous 5-HT1AR/OX1R heterodimers in the rat brain. These antidepressant effects may be mediated by upregulation of BDNF levels and enhanced phosphorylation and activation of CREB in the hippocampus and medial prefrontal cortex. This study provides evidence that 5-HT1AR/OX1R heterodimers are involved in the pathological process of depression. Peptides including TMs of the 5-HT1AR/OX1R heterodimer interface are candidates for the development of compounds with fast-acting antidepressant-like effects